Dark Side of the Moon

David Didlake

Firefighter / Paramedic

Acute Care Nurse Practitioner

@DidlakeDW

Peer review by Dr. Stephen Smith

@smithECGblog

I was reviewing ECG’s in our LifeNet database and happened upon this one without any knowledge of clinical circumstances.

Figure 1

Raw findings include Sinus Rhythm, narrow QRS duration, small q-waves in Leads I / aVL / V5 / V6 (which is not entirely atypical), an inverted P-wave in V1 to suggest possible lead malposition, a normal QRS/T angle, and a dispersion of alternating high and low QRS voltage that would benefit from Echo evaluation to assess the possibility of chamber enlargement.

There is one additional feature – the ST segments of V2-V5 are depressed. When “spot diagnosing” precordial ST-depression I instinctively evaluate aVR for any corresponding ST-elevation to see if an emerging pattern of broad subendocardial ischemia can be appreciated, in which the ST-depression should be otherwise global and demonstrably maximal in Leads II and V5. But in this ECG, Lead aVR is spared of any gross ST changes. Moreover, the ST-depression in V2-V5 is maximal in V3!

A 56 y/o Male called 911 from his hotel room in the early morning hours after abruptly awakening from sleep with crushing chest discomfort and difficulty breathing. He reported to EMS a medical history of GERD only. The physical exam was unremarkable for diaphoresis or pallor, and he denied any episodes of vomiting. Furthermore, there was no family history of early CAD, MI, or sudden cardiac death.

• BP 142/100

• HR 90

• RR 16 (BBS CTA)

• SpO2 99 (RA)

• Dstick 110

My colleagues noted the ST-depression in the respective leads, as well, and STEMI activated to the nearest PCI center. The patient was administered 324mg ASA, and serial ECG’s were conducted with most, unfortunately, imperiled by artifact. This final ECG, however, was recorded upon hospital arrival, the timing of which coincided with the patient verbalizing cessation of symptoms.

Figure 2

V5 / V6 = V8 / V9, respectively

The ST-depression in V2-V4 has lessened with near restoration to baseline. What about V8-V9? Do they show anything noteworthy? Is posterior lead placement even necessary? There is currently zero ST-elevation here, but not because it never existed; rather, this ECG has been recorded during a time in which the ST-depression of V2-V4 has acutely resolved. Thus, one can't dismissively say that the posterior leads are truly negative. Well, they certainly are at this moment (due to reperfusion, further detailed below) but they just as easily might have been earlier during maximal ST-depression in V2-V4. We don't know because they weren't recorded at that time. This isn't entirely paradoxical, because here is something to remember -- ischemic changes that induce electrical alterations on the ECG must travel through lung volume before reaching the posterior leads. There is a natural voltage attenuation associated with this. V8-V9 intermittently capture ST changes, but not consistently.

Notice that the T-waves in V2-V4 are more pronounced, more upright, and slightly wider at the base. In previous posts we have investigated this very kind of T-wave and that these features should raise suspicion of hyperacuity. However, in this context (i.e. cessation of symptoms), and in this unique territory (V2-V4), the T-wave characteristics are consistent with posterior reperfusion! [1]

Here is the admitting ED ECG after cancellation of Code STEMI.

• V2 – in the final EMS ECG the ST segment was baseline. Here the J-point hovers just above the PQ junction with an even more defined T wave in terms of height and width.

• V3 – in the final EMS ECG the ST segment was still slightly depressed. Here it is now baseline with similar T-wave characteristics as that of V2.

• V4 – the ST segment is baseline with an associated wider, and taller, T wave.

The patient continued to verbalize cessation of symptoms while in the ED. Cardiology admitted him for observation with plans for next-day coronary angiogram. No other ECG’s were recorded, unfortunately, and I was unable to ascertain any specifics as to whether or not his pain returned, or remained controlled.

The Troponin I peaked at 13 ng/mL (Hospital Dx NSTEMI), and while preparing for Cath he requested to leave the hospital and return home (out of town) to see his personal physician. He left AMA and is lost to follow-up.

Posterior OMI is typically by means of extension from a more apparent injury presentation (e.g. ST-elevation, Hyperacute T waves, etc.) in the inferior, or lateral, leads. A truly isolated posterior OMI, however, is thought to be rare. [2] In fact, in the cited literature, van Gorselen reported that the incidence may be as little as 3%. But this percentage value might increase when tactics described below are deployed, thus showing that isolated posterior OMI is not as rare as previously considered, after all, but rather victim to dismissive categorization of non-occlusive ischemia.

We can backtrack to the original time-zero ECG (Figure 1) and determine if any apparent inferior, or lateral, primary injury manifestation (e.g. ST-elevation, etc.) is present.

Collective assessment of both inferior and lateral territory discloses no findings of ST-elevation, or Hyperacute T waves. There is a small chance that the terminal QRS deflection in Lead II is a delayed action wave (DAW), which is considered to be a Q-wave equivalent [3, 4], however this finding is limited to Lead II only and there is beat-to-beat variability here which potentially undermines the consideration of such as a plausible finding.

Even if not applicable in this case I like to consider the DAW, still, when the injury pattern at the very least appears to be isolated to the posterior wall. The DAW is defined as:

• A notch / deflection in the terminal QRS

• The height of the notch is greater than, or equal to, 2mm (comparison to PR)

• Disappearance of notch in 24 hours

• Slight QRS prolongation in leads where the notch is found

• Typically seen in Leads II, III, aVF, or I, aVL (associated with LCx occlusion)

Anecdotally, van Gorselen strongly advocated deployment of Leads V7-V9 when holding suspect an isolated posterior wall OMI. Attached is the ECG from his paper with these leads applied.

Yes, there is demonstrable ST-elevation amidst lead reconfiguration to the posterior wall. But there is, also, something else – what I believe to be DAW’s in II / III / aVF. The patient in the van Gorselen report received PCI for a 90% LCx occlusion.

Surveilling for the presence of DAW’s, or applying posterior leads, is probably not necessary when the precordial ST-depression is most profound in V1-V4, whether in isolation or associated with more global ST-depression in other leads. Smith and Meyers found that patients presenting with high-risk ACS and any ST-depression, even less than 1 mm, maximal in leads V1-V4 to be 97% specific for OMI and 96% specific for OMI requiring emergent PCI. [5]

The time-zero ECG (Figure 1) in today’s case is consistent with Posterior OMI, regardless of how rare the incidence is thought to be, that eventually resolves with stereotypical posterior reperfusion T waves (Figure 3). As previously mentioned, there is no grossly apparent ST-elevation, or Hyperacute T waves, in the inferior or lateral territory, to coincide with this. Additionally, there is no reliable demonstration of DAW’s. However, amidst the ST-depression V2-V5 it is maximal in V3, effectively eliminating any need for posterior wall lead placement.

The EMS crews were correct moving forward with STEMI activation. The peak Troponin I confirmed myocardial infarction. (A peak Troponin I > 10 ng/mL is very specific for occlusion MI.) Unfortunately, due to the patient’s abrupt exodus from the PCI center – without benefit of coronary angiogram, or echo, for example – the disposition will forever remain unknown.

[1] Driver, B. E., et al. (2016). Posterior wall reperfusion T-waves: Wellens’ syndrome of the posterior wall. Emergency Medicine Journal, 1-5.

[2] van Gorselen, E., et al. (2007). Posterior myocardial infarction: The dark side of the moon. Netherlands Heart Journal, 15 (1), 16-21.

[3] Niu, T., et al. (2011). The delayed action wave in non-ST-elevation myocardial infarction. International Journal of Cardiology, 162, 107-111.

[4] Yang, T., et al. (2019). Non-ST-elevated myocardial infarction with “N” wave on electrocardiogram and culprit vessel in left circumflex has a risk equivalent to ST-elevated myocardial infarction. Clinical Cardiology, 43, 491-499.

[5] Meyers, H. P., et al. (2021). Ischemic ST-segment depression maximal in V1-V4 (versus V5-V6) of any amplitude is specific for occlusion myocardial infarction (versus nonocclusive ischemia). Journal of the American Heart Association, 10, 1-4.